Search results for "endothelium"

showing 9 items of 749 documents

Endothelin action on goat cerebral arteries.

1990

Abstract Cumulative application of endothelin-1 (human) markedly constricted goat isolated cerebral arteries in a concentration-dependent manner. Contractile responses were not affected by removal of endothelial cells. Removal of extracellular calcium or addition of the calcium channel blocker nicardipine (10−7 M) failed to abolish responses to endothelin. The results suggest that the endothelium-independent constriction of cerebral arteries produced by endothelin cannot be explained solely by voltage-dependent calcium channels. The contractile responses are likely to be mediated by stimulation of specific receptors for this peptide.

medicine.medical_specialtymedicine.drug_classCerebral arteriesNicardipinePharmaceutical Sciencechemistry.chemical_elementStimulationCalcium channel blockerBiologyCalciumIn Vitro TechniquesMuscle Smooth VascularNicardipineInternal medicinemedicineAnimalsPharmacologyVoltage-dependent calcium channelEndothelinsGoatsCerebral ArteriesEndocrinologymedicine.anatomical_structurechemistrycardiovascular systemCalciumFemaleEndothelium VascularEndothelin receptormedicine.drugBlood vesselMuscle ContractionThe Journal of pharmacy and pharmacology
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Cigarette smoke-induced pulmonary endothelial dysfunction is partially suppressed by sildenafil.

2009

Abstract Cigarette smoke mediated oxidative stress and endothelial dysfunction are important processes in the pathogenesis of several lung disorders. In this study we evaluated the effect of PDE5 inhibition on pulmonary artery endothelial dysfunction induced by cigarette smoke in vitro . Human pulmonary artery endothelial cells (HPAEC) were incubated in the absence or presence of PDE5 inhibitor sildenafil (10 nM–1 μM), PKG agonist 8-Br-cGMP (1 mM), or the antioxidants dyphenyleneiodonium (DPI 1 μM) and N -acetylcysteine (NAC 1 mM) for 30 min. Then, cigarette smoke extract (CSE) was added for 24 h. CSE (2.5–10%)-induced ROS generation was suppressed by DPI, and partially reversed by sildenaf…

medicine.medical_specialtymedicine.drug_mechanism_of_actionSildenafilVasodilator AgentsPharmaceutical ScienceEnzyme-Linked Immunosorbent Assaymedicine.disease_causeNitric OxidePolymerase Chain ReactionPiperazinesSildenafil CitrateAcetylcysteinechemistry.chemical_compoundInternal medicineSmokeparasitic diseasesTobaccomedicineHumansSulfonesEndothelial dysfunctionPhosphodiesterase inhibitorLungCells CulturedDNA PrimersbiologyBase Sequencebusiness.industrymedicine.diseaseEndothelial stem cellEndocrinologychemistryEnzyme inhibitorPurinescardiovascular systembiology.proteinEndothelium VascularbusinessPhosphodiesterase 5 inhibitorOxidative stressmedicine.drugEuropean journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences
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Interleukin-6 production in "normal" and HTLV-1 tax-expressing brain-specific endothelial cells.

1993

Abnormal cytokine production can contribute in many instances to the development of pathology. Our study focuses on the regulation of interleukin (IL)-6 production in vitro in brain-specific endothelial cells (BEC) under physiological conditions and in a model of human T leukemia virus-1 (HTLV-1) infection. IL-6 production was strongly up-regulated in a dose-dependent mode upon exposure to recombinant IL-1 beta, although nearly not detectable in unstimulated BEC. This induction of IL-6 production could be achieved by reagents known to increase intracellular levels of cAMP, such as forskolin, prostaglandin E or pentoxifylline. Furthermore, transcription and production of IL-6 was inducible b…

medicine.medical_specialtymedicine.medical_treatmentImmunologyTransfectionchemistry.chemical_compoundMiceInternal medicinemedicineImmunology and AllergyAnimalsRNA MessengerInterleukin 6health care economics and organizationsCells CulturedMice Inbred BALB CForskolinbiologyInterleukin-6Genes pXInterleukinBrainTransfectionHTLV-I InfectionsCell biologyEndothelial stem cellCytokineEndocrinologychemistryBucladesineSecond messenger systembiology.proteinEndothelium VascularProstaglandin EEuropean journal of immunology
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The soluble terminal complement complex (SC5b-9) up-regulates osteoprotegerin expression and release by endothelial cells: Implications in rheumatoid…

2009

Objective. Complement activation products contribute to a large number of inflammatory diseases, including RA. We have investigated whether osteoprotegerin (OPG) may concur with the soluble terminal complement complex (SC5b-9) to the inflammatory cascade characterizing RA. Methods. Levels of SC5b-9 and OPG in the plasma and SF of patients with active RA were determined by ELISA. The presence of SC5b-9 and OPG in RA synovial lesions was analysed by immunohistochemistry. Cultured endothelial cells were used for in vitro leucocyte/endothelial cell adhesion assays. In addition, endothelial cells were exposed to SC5b-9 in order to evaluate the effects on the production of OPG protein, as well as…

musculoskeletal diseasesAdultMalemedicine.medical_specialtyComplement systemEndotheliumNeutrophilsArthritisInflammationComplement Membrane Attack ComplexArthritis RheumatoidEndothelium; Osteoprotegerin; Inflammation; Complement systemRheumatologyOsteoprotegerinInternal medicineCell AdhesionMedicineHumansPharmacology (medical)EndotheliumCells CulturedAgedInflammationEndothelial CellDose-Response Relationship Drugbusiness.industryNeutrophilSynovial MembraneOsteoprotegerinEndothelial CellsMiddle Agedmedicine.diseaseIn vitroComplement systemUp-RegulationEndothelial stem cellEndocrinologymedicine.anatomical_structureNeutrophil InfiltrationFemaleComplement system; Endothelium; Inflammation; Osteoprotegerin; Adult; Aged; Arthritis Rheumatoid; Cell Adhesion; Cells Cultured; Complement Membrane Attack Complex; Dose-Response Relationship Drug; Endothelial Cells; Endothelium Vascular; Female; Humans; Male; Middle Aged; Neutrophil Infiltration; Neutrophils; Osteoprotegerin; Synovial Membrane; Up-Regulation; Rheumatology; Pharmacology (medical)Endothelium Vascularmedicine.symptombusinessComplement membrane attack complexHuman
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Bindungsstudien mit Ulex Europaeus Agglutinin I (UEA-I) am Gefäßendothel der Synovialmembran*

2008

The lectin binding sites of the synovium of patients with rheumatoid arthritis and osteoarthritis were investigated. It was shown that Ulex europaeus agglutinin is a constant marker of the vascular endothelium and is not induced during the course of inflammatory process in rheumatoid arthritis.

musculoskeletal diseasesPathologymedicine.medical_specialtybiologyEndotheliumChemistryArthritisOsteoarthritismedicine.diseasebiology.organism_classificationUlex europaeusVascular endotheliumAgglutininmedicine.anatomical_structureRheumatoid arthritisLectin bindingImmunologymedicineOrthopedics and Sports MedicineSurgeryskin and connective tissue diseasesZeitschrift für Orthopädie und ihre Grenzgebiete
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Physical inactivity increases oxidative stress, endothelial dysfunction, and atherosclerosis.

2005

Objective— Sedentary lifestyle is associated with increased cardiovascular events. The underlying molecular mechanisms are incompletely understood. Reactive oxygen species (ROS) contribute to endothelial dysfunction and atherosclerosis. An important source of vascular ROS is the NADPH oxidase. Methods and Results— C57BL6 mice were subjected to regular housing (physical inactivity) or voluntary training on running wheels (6 weeks). Inactivity increased vascular lipid peroxidation to 148±9% and upregulated superoxide release to 176±17% (L-012 chemiluminescence) and 188±29% (cytochrome C reduction assay), respectively. ROS production was predominantly increased in the endothelium and the medi…

rac1 GTP-Binding Proteinmedicine.medical_specialtyEndotheliumNitric Oxide Synthase Type IIIArteriosclerosisNitric Oxide Synthase Type IIBiologymedicine.disease_causechemistry.chemical_compoundMiceApolipoproteins EInternal medicinePhysical Conditioning AnimalmedicineAnimalsNADH NADPH OxidoreductasesRNA MessengerEndothelial dysfunctionLife Stylechemistry.chemical_classificationReactive oxygen speciesNADPH oxidaseSuperoxideNeuropeptidesNADPH Oxidase 1NADPH Oxidasesmedicine.diseasePhosphoproteinsMice Mutant Strainsrac GTP-Binding ProteinsMice Inbred C57BLVasodilationOxidative Stressmedicine.anatomical_structureEndocrinologychemistryNOX1biology.proteinNADPH Oxidase 1Endothelium VascularNitric Oxide SynthaseCardiology and Cardiovascular MedicineReactive Oxygen SpeciesOxidative stressArteriosclerosis, thrombosis, and vascular biology
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Lovastatin inhibits Rho-regulated expression of E-selectin by TNFalpha and attenuates tumor cell adhesion.

2003

E-selectin mediated cell-cell adhesion plays an important role in inflammatory processes and extravasation of tumor cells. Tumor necrosis factor-alpha (TNF-alpha) induces E-selectin gene and protein expression in primary human endothelial cells (HUVEC) and in an endothelial cell line (EA.hy-926). As shown by ELISA and FACS analyses, HMG-CoA reductase inhibitors (e.g., lovastatin) impair the TNF-alpha stimulated increase in E-selectin protein expression. Similar results were obtained for E-selectin mRNA expression and promoter activity, indicating that the effect of lovastatin is based on inhibition of gene expression. The effective inhibitory concentration of lovastatin was in a physiologic…

rho GTP-Binding ProteinsRHOATranscription GeneticRHOBAntineoplastic AgentsBiochemistryCell MovementCell Line TumorNeoplasmsGene expressionE-selectinGeneticsmedicineCell AdhesionHumansLovastatinCell adhesionMolecular BiologyCells CulturedbiologyTumor Necrosis Factor-alphaCell biologybiology.proteinCancer researchTumor necrosis factor alphaLovastatinEndothelium VascularSignal transductionE-SelectinBiotechnologymedicine.drugSignal TransductionFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Genetic Factors as Promising Biomarkers of Sporadic Ascending Aortic Aneurysm

2014

Thoracic aorta shows various changes with advancing age and a progressive deterioration in structure and function. As a result, vascular remodeling (VR) and medial degeneration (MD) occur. VR and MD are typical entities of sporadic thoracic aortic aneurysm (TAA), actually considered a common and serious health risk and a pathology by unclear mechanisms. Increased activity of the coagulation system, inflammation, activation of extracellular matrix remodeling and endothelial dysfunction pathways have been recently evidenced to have a key role in its onset. Thus, polymorphisms of the coagulation system [fibrinogen (rs1800790); Factor II ( rs1799963); Factor V (rs6025); Factor VII (rs121964926)…

tPA ( rs2020918)ACE (rs1799752)]PAI-1 (rs1799768)TAFI (rs2146881)] inflammation [TLR4 (rs4986790)Factor V (rs6025)CCR5 (rs333)] extra-cellular matrix remodeling [MMP9 (rs3918242)vascular remodeling (VR) and medial degeneration (MD)sporadic thoracic aortic aneurysm (TAA)polymorphisms of the coagulation system [fibrinogen (rs1800790)MMP2 (rs243865)] endothelium dysfunction [eNOs (rs 1799983)Factor II ( rs1799963)Factor VII (rs121964926)
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Ultraviolet A1 radiation induces nitric oxide synthase-2 expression in human skin endothelial cells in the absence of proinflammatory cytokines.

2001

Skin exposure to ultraviolet radiation from sunlight causes erythema and edema formation as well as inflammatory responses. As some of these ultraviolet-induced effects are potentially mediated by nitric oxide synthases, we examined the role of cytokines and ultraviolet A 1 radiation (340–400 nm) on the expression of the nitric oxide synthase-2 in endothelia of normal human skin biopsies during short-term organ culture as well as expression and activity of the nitric oxide synthase-2 in in vitro cell cultures of human dermal endothelial cells. Both, cytokine challenge (interleukin-1β + tumor necrosis factor-α + interferon-γ) but also ultraviolet A 1 exposure (50 J per cm 2 ) in the absence …

ultraviolet A1Ultraviolet Raysmedicine.medical_treatmentNitric Oxide Synthase Type IIHuman skinInflammationDermatologyBiologyBiochemistryProinflammatory cytokineNitric oxideCell Linechemistry.chemical_compoundInterferon-gammanitric oxidemedicineHumansEndotheliumPromoter Regions GeneticMolecular BiologySkinTumor Necrosis Factor-alphaNitric oxide synthase 2Cell BiologyMolecular biologynitric oxide synthase-2endothelial cellsNitric oxide synthasehealing cytokinesCytokinechemistryEnzyme InductionImmunologybiology.proteinCytokinesTumor necrosis factor alphamedicine.symptomhuman skinInflammation MediatorsNitric Oxide SynthaseInterleukin-1The Journal of investigative dermatology
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